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American Journal Of Biomedical Science & Pharmaceutical Innovation    
(ISSN – 2771-2753) 
VOLUME 04 ISSUE 07 PAGES: 33-48 

OCLC – 1121105677     

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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ABSTRACT 

Relevance: Understanding of the molecular and genetic mechanisms underlying acne and acne scar formation is still 

in its infancy. However, ongoing research in this area increases our knowledge of disease mechanisms and may 

contribute to the development of new preventive and treatment strategies. Research confirms the significant role of 

genetic factors in the development of acne, affecting its occurrence, course and effectiveness of treatment. Particular 

attention is paid to gene polymorphisms associated with inflammation, androgen metabolism and the immune 

response, such as CYP17A1 and TNF-α. These data highlight the importance of taking patients' genetic profile into 

account when diagnosing and choosing therapy, which can improve treatment outcomes and prevent disease relapse. 

Based on an analysis of literature data, in Uzbekistan there is insufficient understanding of the prognostic significance 

and role of the NLR and TLR2 genes in the development of acne. This highlights the complexity of the genetic 

component of acne and indicates the need for additional research to better understand the influence of these and 

other genetic factors on the pathogenesis of the disease. 

Conclusion. An in-depth study of the genetic aspects of acne will not only enrich the scientific understanding of the 

disease, but will also open up new opportunities for its more effective treatment and prevention. 

KEYWORDS 

Acne, molecular genetic mechanisms, kelliod, prognosis. 

  Research Article 

 

THE ROLE OF GENETIC MUTATIONS IN THE DEVELOPMENT OF ACNE 
 

Submission Date: July 21, 2024, Accepted Date:  July 26, 2024,  

Published Date: July 31, 2024  

Crossref doi: https://doi.org/10.37547/ajbspi/Volume04Issue07-05 

 

 

Khamidova Farida Muinovna  
Samarkand State Medical University, Department of Pathological Anatomy with a sectional course, Uzbekistan 

 

Khusinova Firuza Azgar Kizi 
Samarkand State Medical University, Department of Pathological Anatomy with a sectional course, Uzbekistan 

 

Journal Website: 

https://theusajournals.

com/index.php/ajbspi 

Copyright: Original 

content from this work 

may be used under the 

terms of the creative 

commons attributes 

4.0 licence. 

 

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INTRODUCTION

Acne (L70, L73. 0.) is a chronic inflammatory skin 

disease affecting the hair sebaceous follicles and is 

caused by a variety of factors including genetics and 

androgens. Neonatal acne (acne neonatorum) occurs 

in the first four weeks of life, and infantile acne appears 

between 3 and 6 months. These conditions may be 

associated with high androgen levels in girls and boys 

(1,7). 

Acne can develop at any age and is often seen in 

teenagers and young adults. Symptoms include 

comedones, pustules and inflammatory nodules. 

Microbial flora, in particular Cutibacterium acnes, plays 

a significant role in pathogenesis, causing 

inflammation and infection. 

Treatment for acne includes topical retinoids, benzoyl 

peroxide, antibiotics and, in some cases, oral 

contraceptives or isotretinoin. It is important to 

consider antibiotic resistance and the potential 

psychological effects of the disease (2,8). 

Historically, acne has been known since ancient times; 

its descriptions are found among the ancient Egyptians 

and Greeks. Current understanding of the disease 

emphasizes the importance of genetic and immune 

factors in its development. 

Acne is an inflammatory skin disease that can appear at 

different points in life and is often associated with 

genetic factors (1,2,3,4). 

Neonatal, nodular cystic and conglobate acne have a 

pronounced genetic predisposition, and acne after 

adolescence is associated with a family history of acne 

in 50% of cases. 

Research has identified genetic markers associated 

with acne, including apolipoprotein A1 and various loci 

detected through genome-wide analyses. Several 

genetic pathways, including PI3K/AKT/mTOR, may 

regulate sebum production and inflammation, which 

play a key role in the development of acne (5). 

Acne severity scoring systems vary and may include 

analysis of comedones, papules and pustules. 

Immunity research has shown that inflammation in 

acne can be caused by a variety of factors, including 

skin microbes and innate immune responses. 

The following clinical and morphological forms of acne 

are distinguished: 

L70.0- Common acne (acne vulgaris), L70.1 - Globular 

acne, L70.2 Smallpox acne, Necrotic miliary acne, L70.3- 

Tropical acne, L70.4-Children's acne, L70.5- Acne 

excoriée, Excoriated acne, L70.5-Other acne, L70.9-

Acne, unspecified. 

Acne Vulgaris is a globally common chronic 

inflammatory disease of the hair and sebaceous 

follicles. Although acne is not life-threatening, it can 

cause scarring, irritation and serious psychological 

problems, including depression. Our review examines 

the various causes of acne and methods of treating 

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them. Major pathophysiological factors include 

excessive sebum production, hyperkeratinization, P. 

acnes colonization, and inflammation. In diagnosing 

acne, it is important to distinguish between 

inflammatory and non-inflammatory forms of lesions. 

Problems of antibiotic resistance require the 

development of new treatments (12). 

Epidemiological studies show that acne affects up to 

80% of adolescents and young adults. The age at which 

acne most often begins ranges from 14 to 16 years in 

girls and 16 to 17 years in boys. However, although acne 

affects men and women at approximately the same 

frequency, severe forms are more common among 

men (17,18,19,20,21,22). 

The causes and mechanisms of acne development are 

not fully understood, but they are believed to be 

associated with a number of factors. These include 

hormonal imbalance and hypersecretion of sebum, 

changes in its chemical composition, follicular 

hyperkeratosis and colonization of the skin by the 

bacteria Propionibacterium acnes. An important role in 

the development of acne belongs to the immune 

response to the antigens of these microorganisms, 

which activate neutrophils and phagocytes. 

 These cells stimulate the complement system through 

Toll-like receptors (TLR2), resulting in the synthesis of 

pro-inflammatory interleukins such as IL-8, TNF-α, IL-1β 

and IL-12. These interleukins activate cyclooxygenase, 

which promotes the production of inflammatory 

mediators, such as leukotriene B4 from arachidonic 

acid. It has been established that leukotriene B4 

activates monocytes, eosinophils, T-lymphocytes and 

other cells that secrete hydrolytic enzymes that 

destroy the wall of the sebaceous gland. This leads to 

the release of the contents of the gland into the 

surrounding tissues and causes the development of 

inflammation at the site of the lesion (23,24). 

Immunodeficiencies such as chronic granulomatous 

disease (CGD) can aggravate skin conditions such as 

folliculitis. CGD is a rare inherited disease caused by a 

defect in the enzyme NADPH oxidase, which prevents 

white blood cells from effectively killing pathogens. 

Such patients may experience recurrent bacterial and 

fungal skin infections, including folliculitis and acne. 

Diagnosis of CGD involves specific tests for neutrophil 

function, and treatment includes infection prevention 

and immunomodulators (6,7,8). 

Hidradenitis suppurativa, also known as acne inversus 

or acne inversus, is a chronic inflammatory skin disease 

affecting the hair follicles and is associated with acne. 

The disease manifests in intertriginous areas and can 

cause significant burden due to pain, itching, malodor, 

and emotional distress. Treatment may include 

antibiotics, antimicrobials, and surgical interventions 

to control symptoms and prevent disease progression 

(9,10,11). 

A study by Ballanger et al shows a significant influence 

of heredity on the development and course of acne. A 

family history of acne (A+) is associated with earlier 

onset of the disease, often before puberty, and 

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increases the recurrence rate after isotretinoin 

treatment. In addition, acne patients whose parents 

also suffered from acne (M+ and M+F+) are more likely 

to experience problems with retention lesions. This 

highlights the role of genetic factors as an important 

prognostic indicator in clinical practice in the diagnosis 

and selection of treatment strategies for acne (15). 

Modern research focuses on the genetic aspects of 

acne, indicating that genetic predisposition 

significantly influences the occurrence, clinical 

presentation, course and effectiveness of acne 

treatment. Acne is a polygenic disease, which means 

that it does not follow the classical laws of Mednellian 

inheritance (25,26). 

There are many genetic markers associated with acne, 

including polymorphisms in genes such as tumor 

necrosis factor alpha, matrix metalloproteinases 

(MMPs), tissue inhibitors of metalloproteinases 

(TIMPs), interleukin-1, CYP17A1, CYP1A1, and others. 

Research by Yaykasli K.O. showed that genotype 

frequencies for matrix metalloproteinase-2 (MMP-2) 

and TIMP-2 inhibitor polymorphisms were similar in a 

Turkish population between acne patients and 

controls. However, an imbalance between MMPs and 

TIMP-2 may increase susceptibility to acne, as shown 

for the TIMP-2 (-418 C/C) genotype, which was twice as 

common in patients compared to controls (27). 

Most of the genes studied in the context of acne play 

key roles in innate immune function, skin lesion 

formation, or steroid hormone metabolism. Particular 

attention is paid to polymorphisms of genes involved 

in the biosynthesis of androgens, including 

testosterone, such as cytochrome P450c17α, encoded 

by the CYP17A1 gene (28,29,30,31,32). 

A study by N. Malikova et al. in the Uzbek population 

showed that certain genotypic variants of the CYP17A1 

gene are associated with a higher likelihood of 

developing acne and its severe course. For example, 

the heterozygous A/G genotype was typical for 

patients with moderate acne, while the G/G genotype 

was more common in patients with severe acne. The 

A/A variant was protective and associated with a 

reduced risk of acne (33,34). 

In China, the CYP17-34T/C polymorphism was 

associated with acne, with men with the homozygous 

C/C variant and the C allele having a high risk of severe 

acne, in contrast to women with mild to moderate 

acne, where no such association was observed (35 ,36). 

A polymerase chain reaction (PCR) study examined the 

effect of CYP17 gene polymorphisms on the 

development of acne in Chinese men. The homozygous 

C/C variant and the C allele were found to be 

significantly more common in men with severe forms 

of acne compared to the control group, confirming 

statistically significant differences. However, among 

women with mild and moderate forms of acne, no 

statistically significant differences were found with the 

control group, indicating a possible sex difference in 

the genetic predisposition to severe forms of acne. 

Another study among Indonesian patients showed 

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that polymorphisms in the CYP17A1, CYP1A1 and TNF-α 

genes did not correlate with the risk of developing 

severe acne. However, it has been found that 

polymorphisms in the CYP1A1 gene may contribute to 

acne in general. These findings highlight the 

complexity of the genetic background of acne and the 

need for further research to determine the precise role 

of these and other genetic factors in the development 

of the disease (37). 

Researchers in Germany found that having the GG 

genotype of the CYP1A1 gene may increase the risk of 

developing acne. This genotype is thought to 

contribute to a deficiency of natural retinoids leading 

to follicular hyperkeratosis and acne vulgaris. This may 

also explain the high effectiveness of retinoids in the 

treatment of severe acne in patients with this 

polymorphism, since they show a better therapeutic 

response than patients without this polymorphism 

(38). 

Studies have shown that the -308 G/A and -238 G/A 

polymorphisms in the TNF gene are significantly more 

common in patients with acne vulgaris, especially 

those suffering from severe forms of acne, than in 

healthy individuals. This is confirmed by the increased 

risk of developing acne in the European population 

compared to the Asian population. In addition, high 

levels of the proinflammatory cytokine IL-8 and a 

significant frequency of the IL-8-251T>A polymorphism 

are found in Pakistani patients with acne, highlighting 

a genetic predisposition to the development and 

severity of acne (39,40,41,42). 

In addition, analysis of the rs4646421 polymorphism of 

the CYP1A1 gene showed that although the activity of 

the cytochrome CYP1A1 enzyme is important for the 

metabolism of sex hormones and vitamin A, a direct 

connection of this polymorphism with the 

development of acne was not found. However, this 

genetic marker has been shown to have significant 

prognostic value for predicting severe acne, as patients 

with severe acne are more than twice as likely to have 

an unfavorable allelic variant as controls (43). 

An increase in the level of TSPO in the skin of patients 

with acne, along with other enzymes that metabolize 

steroids - 3βHSD, CYP11A1, may indicate an 

intensification of the synthesis of steroids in the skin 

during this period. Pathology, as well as their 

contribution to the development of chronic 

inflammation in acne (50). 

A study from Western Iran found that the PPARγ 

Pro12Ala and C161T polymorphisms do not directly 

influence the risk of developing acne vulgaris (AV), but 

the PPARγ Pro allele is associated with increased 

susceptibility to AV in adults over 20 years of age. In 

addition, polymorphisms influence the lipid profile of 

patients, indicating significantly higher levels of total 

cholesterol and triglycerides in carriers of the variant 

CG genotype compared to the CC genotype. The study 

also found that CT and TT genotypes were associated 

with lower serum cholesterol and LDL-C levels. These 

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data highlight the importance of genetic factors in the 

pathogenesis and clinical presentation of acne, as well 

as their possible influence on the lipid profile, which 

may have implications for the choice of acne treatment 

strategy (16). 

A study conducted among Turkish patients with acne 

vulgaris found significant differences in the frequency 

of the IGF-I (CA)19 genotype between affected and 

healthy subjects, supporting its possible influence on 

the development of acne (P=0.0002). This genotype 

was also found to be associated with acne severity 

(P=0.015), suggesting a role in disease progression in 

this ethnic group (44,45). 

Studies have also shown that tumor necrosis factor 

alpha (TNF-α), a powerful pro-inflammatory cytokine, 

plays a key role in triggering and regulating the 

cytokine cascade in inflammation and the immune 

response. One of the functional polymorphic loci, G-

308A, has a significant effect on the synthesis and level 

of TNF-α in the body, which emphasizes its potential 

importance in the pathogenesis of acne and its clinical 

course (46,47). 

The authors concluded that elevated levels of 

interleukin-8 and its genetic polymorphism IL-8-251T>A 

may contribute to the development of acne in the 

population. Genetic markers play a key role in the 

development and progression of acne. A detailed study 

of the genetic and immunogenetic factors associated 

with acne may lead to a better understanding of the 

molecular and genetic mechanisms of this condition. 

This knowledge will help in the development of new 

methods to predict the course of the disease and 

effective therapeutic approaches to treat acne, taking 

into account genetic polymorphisms (48,49). 

The formation of scar tissue includes three phases that 

follow in a certain time sequence: inflammatory, 

proliferative and remodeling phase (51). 

The main structural units active in the inflammatory 

and proliferative phase are fibroblasts, capillary 

endothelium, transform-transient growth factor (TGF) 

β1 and β2, platelet-derived growth factor (PDGF), 

insulin-like growth factor (IGF-1) and epidermal growth 

factor (EGF). Vascular endothelial growth factor 

(VEGF), which is produced by epidermal cells, acts as a 

positive regulator of angiogenesis. Tissue inhibitors of 

metalloproteinases (TIMPs) are endogenous inhibitors 

of matrix metalloproteinases (MMPs). Thus, increased 

levels of TIMP are presumably associated with 

hypertrophic scar formation. Tumor necrosis factor α 

(TNF-α) is an inflammatory cytokine produced by 

monocytes and macrophages during the inflammatory 

phase. This cytokine is known to cause collagen 

degradation and help minimize excessive scarring (52). 

During the remodeling phase, excess extracellular 

matrix is degraded and type III collagen, the immature 

form of collagen, is replaced by mature type I collagen. 

TGF-β3 is believed to play a leading role in this process. 

Also, members of the MMP family have a significant 

effect on the degradation and remodeling of the ECM 

and mediate the degradation of collagen types I and III, 

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reducing inflammation and neutralizing the effects of 

chemokines (53). 

Decorin is a proteoglycan component of cutaneous 

connective tissue that binds to type I collagen fibrils 

and influences TGF-β. By binding and neutralizing TGF-

β, decorin reduces the stimulating effect of TGF-β on 

the synthesis of collagen, fibronectin and 

glycosaminoglycan. Decorin levels are reduced in 

keloids and hypertrophic scars, and its antifibrotic 

properties have attracted attention as a possible 

therapeutic agent (54,55). 

The role of periosteum (extracellular matrix protein), 

the level of which is sharply increased in hypertrophic 

scars and keloids compared to normal tissues, is also 

actively discussed (56,57). 

Proinflammatory factors such as interleukins IL-1α, IL-

1β, IL-6, and tumor necrosis factor alpha are 

upregulated in keloid tissues, suggesting that patients 

with keloids have increased expression of 

proinflammatory genes in the skin. This may contribute 

to chronic inflammation, which, in turn, can cause 

invasive growth of keloids, although according to the 

results of a study that was conducted in Turkey (90 

people in the study group and 30 in the control group), 

polymorphic variants 

Ants TNF-α (-308 G/A) and IL-1β (-511 C/T) were not 

associated with acne susceptibility, acne scarring, or 

acne severity (58). 

Increased expression of pro-inflammatory factors 

means that keloids and hypertrophic scars are a 

consequence of inflammatory processes in the 

reticular layer of the dermis. Various external and 

internal stimuli (local, systemic and genetic) after injury 

can contribute to inflammation. The nature of these 

irritants most likely determines the characteristics, 

number, and development of keloids and hypertrophic 

scars. In England, when studying a small group of 

patients with keloid scars (including acne), they found 

that the presence of HLADRB5 and HLA-DRB1*15 was 

associated with keloid disease (59). 

A meta-analysis of the association of the Arg72Pro 

polymorphism of the P53 gene with keloid scars in the 

Chinese population included the results of 6 studies, 

which included 359 patients with keloid scars and 493 

people. as a control. It was determined that the Pro 

allele of the Arg72Pro polymorphism of the P53 gene is 

a risk factor for the development of keloids in the 

Chinese population compared to the Arg allele (OR = 

2.29, 95% CI = 1.45–3.60) (60). 

A study was conducted in China in which the first stage 

analyzed 1056 patients with acne and 1056 controls 

using high-density chips. At the second stage of the 

study, in an independent cohort (1860 patients and 

3660 people in the control group), 101 single 

nucleotide polymorphisms were tested, of which 3 

showed an association: rs747650 of the DDB2 gene and 

rs1060573 (11p11.2), rs7531806 of the SELL gene 

(1q24.2), which are involved in androgen metabolism, 

inflammation, and scar formation in severe acne (61). 

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Keloids develop in fibroproliferative disorders against 

the background of chronic inflammatory processes in 

the skin. A genome-wide association study showed an 

association with rs8032158 in the NEDD4 gene. This 

gene is expressed by neural progenitor cells and has six 

different transcripts. Carriage of the rs8032158 risk 

allele C in patients with keloids is associated with 

selectively higher expression of type 3 transcript (TV3 

NEDD4) and activation of the NF-κB pathway. The 

analysis revealed that NEDD4 TV3 is involved in NF-κB 

activation through its association with the adapter 

protein RIP. These results suggest that NEDD4 TV3 is a 

potential diagnostic marker and therapeutic target for 

chronic skin diseases, including keloid (62). 

A genome-wide association study of 478 African 

Americans (122 cases, 356 controls) was conducted in 

the USA in 2014. An association was found with the 

q21.2-22.3 locus on chromosome 15, which includes the 

NEDD4 gene. This gene has previously been shown to 

be associated with keloid scars in Japanese and 

Chinese populations. But in African Americans, a more 

significant association was found with the MYO1E 

gene. In addition, an association was established with 

the q13.5 locus on chromosome 11 (MYO7A gene, 

rs35641839, OR = 4.71, 95% CI 2.38–9.32, p = 8.34 × 10–

6). The authors suggest that the identification of 

polymorphisms associated with the formation of 

keloid scars in two myosin genes indicates that the 

altered cytoskeleton contributes to enhanced 

migratory and invasive properties of keloid fibroblasts 

(63). 

Long non-coding RNAs (lncRNAs) are believed to play 

a significant role in human diseases. Studies have 

shown that overexpression of long non-coding RNA 

AC067945.2 did not affect cell proliferation in 

hypertrophied scar tissue, but promoted early 

apoptosis in normal skin fibroblasts. Except Moreover, 

overexpression of AC067945.2 inhibited the 

expression of COL1A1, COL1A2, COL3A1 and α-SMA 

proteins. In turn, TGF-β1 can inhibit the expression of 

AC067945.2. In the group with overexpression of 

AC067945.2, 138 mRNA expression differed from the 

control group, of which it was increased in 14 and 

decreased in 124. Overexpression of AC067945.2 

correlated with developmental processes, binding, 

extracellular region and the VEGF and Wnt signaling 

pathways. The study revealed the functions of the 

novel lncRNA AC067945.2, which may help understand 

the mechanisms regulated by AC067945.2 in the 

pathogenesis of hypertrophic scars (64).  

Overexpression of long non-coding RNA ncRNA8975-1 

was found in hypertrophic scars and skin fibroblasts. 

Overexpression of lncRNA8975-1 prevents cell 

proliferation and reduces the expression of COL1A2, 

COL1A1, COL3A1 and α-SMA in hypertrophic scar 

fibroblasts, whereas knockdown of lncRNA8975-1 has 

the opposite effect. Further studies of the mechanisms 

by which lncRNA8975-1 expression is regulated may 

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lead to a better understanding of the pathogenesis of 

hypertrophic scars (65). 

The study of the genetic aspects of the problem of scar 

formation after acne, as well as the determination of 

molecular genetic markers of this condition, is almost 

at the very initial stage. It is likely that this gap will be 

filled in the coming years, which will provide impetus 

for the development of new effective means of 

preventing and treating this disease (71). regulators of 

androgen receptors - 25-OH-VD, cytochrome p 450 (17-

alpha hydroxylase), insulin-like growth factor are 

important in the pathogenesis of rapid non-genomic 

molecular cellular reactions of peripheral androgen 

metabolism and, in the future, may determine new 

algorithms for the diagnosis and treatment of acne 

diseases (66). 

An important aspect of acne pathogenesis is the 

participation of keratinocytes in the inflammatory 

response. C. acnes activates Toll-like receptor (TLR)-2 

and TLR-4 on keratinocytes, leading to activation of 

signaling cascades including the NF-κB pathway and 

the MAPK pathway. Subsequently, keratinocytes 

produce IL-1, IL-8, IL-6, granulocyte-macrophage 

colony-stimulating factor (GM-CSF), TNF-α, matrix 

metalloproteinases (MMPs) and human β-defensin-2 

(hBD-2). In addition to TLR-2 and TLR-4, the CD36 

receptor expressed on keratinocytes is also involved in 

the recognition of C. acnes. 

Once C. acnes CD36 is detected, keratinocytes begin to 

synthesize reactive oxygen species (ROS), especially 

superoxide anion, generated from the cytosolic 

enzymes NAD(P)H oxidases. These ROS provide an 

antibacterial effect and trigger an inflammatory 

response. Analysis of identified variants of the 

nucleotide sequence of keratinocyte proliferation and 

differentiation genes showed that severe acne is likely 

associated with polymorphic loci AP3B1, FERMT1, 

FERMT3, GBA, SUFU (67). 

Data on the role of family history and possible 

inheritance of acne have been confirmed in a number 

of studies on familial cases of this dermatosis, its more 

frequent development in monozygotic twins, but the 

significance of genetic associations is not fully known. 

Thus, He L. et al. (2014) revealed a connection between 

acne and TP63, which ensures the regulation and 

differentiation of epithelial stem cells (68). 

 In another study, the authors suggested an 

association of acne development with LGR6, which is a 

mediator of the WNT signaling pathway and ensures 

the functioning and differentiation of sebaceous gland 

stem cells. Additional associated genes were LAMC2, 

encoding a major component of the basement 

membrane, and SPECC1L, encoding a cross-linking 

cytoskeletal protein that plays an important role in cell 

adhesion and migration (69). 

It has been shown that the presence of the disease in 

first-degree relatives may be a risk factor for the 

development of dermatosis. A case of identification 

and determination of the significance of polymorphism 

of the NCF1, CD3E, ORAI1, IGHM, TAZ genes in patients 

https://doi.org/10.37547/ajbspi/Volume03Issue03-01
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with severe forms of the disease with a family history 

is presented. The conducted studies revealed identical 

allelic variants in five genes: NCF1, CD3E, ORAI1, IGHM, 

TAZ in two closely related patients (father and son) 

with severe acne. Polymorphisms of the studied genes 

probably influence the development of an imbalance in 

the oxidase system, the functioning of mitochondria, 

reduced proliferation of T cells, as well as the 

formation of an imbalance in the secretion of 

immunoglobulins. The data obtained may be factors in 

the torpid course of severe dermatosis, which 

determines the need for further research (70). Based 

on the analysis of literature data, it can be noted that 

in our Republic of Uzbekistan, the prognostic values, 

features and role of the NLR and TLR2 genes, and their 

relationship in the development of acne have not been 

fully studied. 

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66. НОВЫЕ ПАТОГЕНЕТИЧЕСКИЕ ФАКТОРЫ 

АНДРОГЕНЗАВИСИМЫХ ДЕРМАТОПАТИЙ. 

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ПОЛИМОРФНЫХ ВАРИАНТОВ ГЕНОВ 

ПРОЛИФЕРАЦИИ И ДИФФЕРЕНЦИРОВКИ 

КЕРАТИНОЦИТОВ ПРИ ТЯЖЕЛОЙ СТЕПЕНИ 

АКНЕ.Демина О.М., Международный научно-

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70. РОЛЬ ГЕНЕТИЧЕСКИХ ФАКТОРОВ ПРИ 

СЕМЕЙНОМ СЛУЧАЕ АКНЕ  О. М. Демина, А. 

Г. Румянцев, Н. Н. Потекаев.ВЕСТНИК РГМУ 

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